Lack of peroxisomal catalase affects heat shock response inCaenorhabditis elegans

Abstract

Exact mechanisms of heat shock–induced lifespan extension, although documented across species, are still not well understood. Here, we show that fully functional peroxisomes, specifically peroxisomal catalase, are needed for the activation of canonical heat shock response and heat-induced hormesis inCaenorhabditis elegans. Although during heat shock, the HSP-70 chaperone is strongly up-regulated in the WT and in the absence of peroxisomal catalase (ctl-2(ua90)II), the small heat shock proteins display modestly increased expression in the mutant. Nuclear foci formation of HSF-1 is reduced in thectl-2(ua90)IImutant. In addition, heat-induced lifespan extension, observed in the WT, is absent in thectl-2(ua90)IIstrain. Activation of the antioxidant response and pentose phosphate pathway are the most prominent changes observed during heat shock in the WT worm but not in thectl-2(ua90)IImutant. Involvement of peroxisomes in the cell-wide cellular response to transient heat shock reported here gives new insight into the role of organelle communication in the organism’s stress response.